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Background: Non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) are caused often by destabilization of non-flow limiting inflamed coronary artery plaques. 18F-fluorodeoxyglucose (FDG) uptake with positron emission tomography/computed tomography (PET/CT) reveals plaque inflammation, while intracoronary optical coherence tomography (OCT) reliably identifies morphological features of coronary instability, such as plaque rupture or erosion. We aimed to prospectively compare these two innovative biotechnologies in the characterization of coronary artery inflammation, which has never been attempted before. Methods: OCT and FDG PET/CT were performed in 18 patients with single vessel coronary artery disease, treated by percutaneous coronary intervention (PCI) with stent implantation, divided into 2 groups: NSTEMI/UA (n = 10) and stable angina (n = 8) patients. Results: Plaque rupture/erosion recurred more frequently [100% vs 25%, p = 0.001] and FDG uptake was greater [TBR median 1.50 vs 0.87, p = 0.004] in NSTEMI/UA than stable angina patients. FDG uptake resulted greater in patients with than without plaque rupture/erosion [1.2 (0.86–1.96) vs 0.87 (0.66–1.07), p = 0.013]. Among NSTEMI/UA patients, no significant difference in FDG uptake was found between ruptured and eroded plaques. The highest FDG uptake values were found in ruptured plaques, belonging to patients with NSTEMI/UA. OCT and PET/CT agreed in 72% of patients [p = 0.018]: 100% of patients with plaque rupture/erosion and increased FDG uptake had NSTEMI/UA. Conclusion: For the first time, we demonstrated that the correspondence between increased FDG uptake with PET/CT and morphology of coronary plaque instability at OCT is high. [ABSTRACT FROM AUTHOR]

Background: Ticagrelor is a reversibly binding, direct-acting, oral, P2Y12 antagonist used for the prevention of atherothrombotic events in patients with coronary artery disease (CAD). Ticagrelor blocks adenosine reuptake through the inhibition of equilibrative nucleoside transporter 1 (ENT-1) on erythrocytes and platelets, thereby facilitating adenosine-induced physiological responses such as an increase in coronary blood flow velocity. Meanwhile, adenosine plays an important role in triggering ischemic preconditioning through the activation of the A1 receptor. Therefore, an increase in ticagrelor-enhanced adenosine bioavailability may confer beneficial effects through mechanisms related to preconditioning activation and improvement of coronary microvascular dysfunction.Methods: To determine whether ticagrelor can trigger ischemic preconditioning and influence microvascular function, we designed this prospective, open-label, pilot study that enrolled patients with stable multivessel CAD requiring staged, fractional flow reserve (FFR)-guided percutaneous coronary intervention (PCI). Participants will be randomized in 1:1 ratios either to ticagrelor (loading dose (LD) 180 mg, maintenance dose (MD) 90 mg bid) or to clopidogrel (LD 600 mg, MD 75 mg) from 3 to 1 days before the scheduled PCI. The PCI operators will be blinded to the randomization arm. The primary endpoint is the delta (difference) between ST segment elevations (in millimeters, mm) as assessed by intracoronary electrocardiogram (ECG) during the two-step sequential coronary balloon inflation in the culprit vessel. Secondary endpoints are 1) changes in coronary flow reserve (CFR), index of microvascular resistance (IMR), and FFR measured in the culprit vessel and reference vessel at the end of PCI, and 2) angina score during inflations. This study started in 2018 with the aim of enrolling 100 patients. Based on the rate of negative FFR up to 30% and a drop-out rate up to 10%, we expect to detect an absolute difference of 4 mm among the study arms in the mean change of ST elevation following repeated balloon inflations. All study procedures were reviewed and approved by the Ethical Committee of the Catholic University of Sacred Heart.Discussion: Ticagrelor might improve ischemia tolerance and microvascular function compared to clopidogrel, and these effects might translate to better long-term clinical outcomes.Trial Registration: EudraCT No. 2016-004746-28. No. NCT02701140.  TRIAL STATUS: Information provided in this manuscript refers to the definitive version (n. 3.0) of the study protocol, dated 31 October 2017, and includes all protocol amendments. Recruitment started on 18 September 2018 and is currently ongoing. The enrollment is expected to be completed by the end of 2019.Trial Sponsor: Fondazione Policlinico Universitario A. Gemelli - Roma, Polo di Scienze Cardiovascolari e Toraciche, Largo Agostino Gemelli 8, 00168 Rome, Italy. [ABSTRACT FROM AUTHOR]

Funding Acknowledgements Type of funding sources: None. Background/Introduction Recently, the transcatheter aortic valve replacement (TAVR) has reformed the management of Aortic Stenosis (AS), providing a valid therapeutic alternative to surgical aortic valve replacement (SAVR). Although optimizing the timing of surgery is a crucial aspiration, the introduction of innovative pharmacological therapies able to modify disease evolution might help clinicians to treat patients in a non-invasive way. Several evidences pointed out the role of inflammation, oxidative stress, and pathological remodelling in AS natural history. Purpose The aim of this study is to assess biological pathways modifications after aortic valve replacement, comparing the transcatheter and the surgical approach. Methods We enrolled a total of 35 consecutive patients with severe symptomatic aortic stenosis undergoing aortic valve replacement with transcatheter (n = 19) or surgical (n = 16) approach. Biological samples were collected and stored before (T0) and 72 hours after the procedure (T1). We firstly performed gene expression arrays for a total of 132 genes, on two groups of pooled cDNA from peripheral blood mononuclear cells of TAVR (n = 10) and SAVR (n = 10) patients. Then, taking into account the most relevant result of the arrays, we selected 15 genes for validation. Results Our preliminary data showed several differences in the gene expression levels of the two groups under examination for a large number of molecules, mostly associated with the oxidative balance. More in detail, after procedure, TAVR patients showed higher levels of glutathione peroxidase 1 (GPX1, TAVR p = 0.029; SAVR p = 0.031) and glutathione reductase (GSR, p = 0.029), while SAVR patients showed higher expression of GPX1, catalase (CAT, p = 0.019) and NADPH oxidase 2 (NOX2, p = 0.008), thus confirming an intense post-operative oxidative stress particularly for patients undergoing surgery. Moreover, Caspase 3 (CASP3, p = 0.013), involved in apoptotic pathway and myocyte enhancer factor 2C (MEF2C, p = 0.036), implicated in overload induced hypertrophy genes showed a significantly reduction in their expression after TAVR. Conclusions In our study, we describe different gene expression signatures in patients with an AS diagnosis and their recalibration after AV replacement with two kinds of procedure, TAVR and SAVR. Our data describe for the first time an altered oxidative balance in patient undergoing aortic valve replacement, that is particularly evident for patients undergoing SAVR. A clearer understanding of biological processes taking place in the first hours post AV replacement lays the ground to a more efficient management of post-operative status and, in the incessant research for a tailored therapy, the results of our study add a little piece of information to assist clinicians in selecting the optimal procedure for each patient. Open in new tab Download slide [ABSTRACT FROM AUTHOR]

OBJECTIVE: To obtain a 'snapshot' view of access-specific percutaneous cardiovascular procedures outcomes in the real world. DESIGN: Multicentre, prospective study performed over a 30-day period. SETTING: Nine hospitals with invasive cardiology facilities, reflecting the contemporary state of healthcare. PATIENTS: Unselected consecutive sample of patients undergoing any percutaneous cardiovascular procedure requiring an arterial access. INTERVENTIONS: Percutaneous cardiovascular procedures by radial or femoral access MAIN OUTCOME MEASURES: The primary outcome was the combined incidence of in-hospital (a) major and minor haemorrhages; (b) peri-procedural stroke; and (c) entry-site vascular complications. The secondary outcome was the combined incidence of in-hospital death and myocardial infarction/reinfarction. For analysis purposes, outcomes were allocated to arterial access-determined study arms on an intention-to treat basis. Multivariable analysis adjusted using propensity score was performed to correct for selection bias related to arterial site. RESULTS: A total of 1052 patients were enrolled: 509 underwent radial access and 543 femoral access. In both groups, 40% underwent a coronary angioplasty. Relative to femoral access, radial access was associated with a lower incidence both of primary (4.2% vs 1.96%, p = 0.03, respectively) and secondary endpoints (3.1% vs 0.6%, p = 0.005, respectively). Multivariate analysis, adjusted for procedural and clinical confounders, confirmed that intention-to-access via the radial route was significantly and independently associated with a decreased risk both of primary (OR 0.37, 95% CI 0.16 to 0.84) and secondary endpoints (OR 0.14, 95% CI 0.03 to 0.62). CONCLUSIONS: Our study indicates strikingly better outcomes of percutaneous cardiovascular procedures with radial access versus femoral access in contemporary, real-world clinical settings. [ABSTRACT FROM AUTHOR]

Objective: To obtain a “snapshot” view of access-specific percutaneous cardiovascular procedures outcomes in the real world. Design: Multicentre, prospective study performed over a 30-day period. Setting: Nine hospitals with invasive cardiology facilities, reflecting the contemporary state of healthcare. Patients: Unselected consecutive sample of patients undergoing any percutaneous cardiovascular procedure requiring an arterial access. Interventions: Percutaneous cardiovascular procedures by radial or femoral access Main outcome measures: The primary outcome was the combined incidence of in-hospital (a) major and minor haemorrhages; (b) peri-procedural stroke; and (c) entry-site vascular complications. The secondary outcome was the combined incidence of in-hospital death and myocardial infarction/reinfarction. For analysis purposes, outcomes were allocated to arterial access-determined study arms on an intention-to treat basis. Multivariable analysis adjusted using propensity score was performed to correct for selection bias related to arterial site. Results: A total of 1052 patients were enrolled: 509 underwent radial access and 543 femoral access. In both groups, 40% underwent a coronary angioplasty. Relative to femoral access, radial access was associated with a lower incidence both of primary (4.2% vs 1.96%, p = 0.03, respectively) and secondary endpoints (3.1% vs 0.6%, p = 0.005, respectively). Multivariate analysis, adjusted for procedural and clinical confounders, confirmed that intention-to-access via the radial route was significantly and independently associated with a decreased risk both of primary (OR 0.37, 95% CI 0.16 to 0.84) and secondary endpoints (OR 0.14, 95% CI 0.03 to 0.62). Conclusions: Our study indicates strikingly better outcomes of percutaneous cardiovascular procedures with radial access versus femoral access in contemporary, real-world clinical settings. [ABSTRACT FROM PUBLISHER]

Objective: To date, no common risk stratification system is available to predict the risk of surgical or percutaneous myocardial revascularisation in patients with coronary artery disease (CAD). Thus, we sought to assess the European System for Cardiac Operative Risk Evaluation (EuroSCORE) validity to predict in-hospital mortality after percutaneous coronary intervention (PCI). Design, setting and participants: EuroSCORE was prospectively and systematically assessed in 1173 consecutive patients undergoing PCI in a high-volume single centre between April 2005 and October 2006. Main outcome measure: The receiver-operating characteristics (ROC) curve was used to describe performance and accuracy of the EuroSCORE risk model for the prediction of in-hospital mortality after PCI. Results: The EuroSCORE model demonstrated an overall relation between EuroSCORE rank and the incidence of in- hospital mortality, showing consistency in predicting patient risk across many subgroups and levels of global risk. At multivariable logistic regression analysis the EuroSCORE value was an independent in-hospital mortality predictor (p = 0.002) together with left main disease (p = 0.005), procedural urgency (p = 0.001), ACC/AHA C type lesion (p = 0.02) and PCI failure (p = 0.01). The area under the ROC curve for the EuroSCORE system was 0.91 (95% CI 0.86 to 0.97), indicating a good ability of the model to discriminate patients at risk of dying during the index hospitalisation. Conclusion: The EuroSCORE risk model, already extensively validated for the prediction of early mortality following open-heart surgery, can also be efficiently utilised in the setting of PCI. The introduction of the EuroSCORE assessment in patients with documented CAD may help to improve the revascularisation strategy decision-making process. [ABSTRACT FROM AUTHOR]